Redefining oxidative stress in Alzheimer's disease: Targeting platelet reactive oxygen species for novel therapeutic options

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dc.contributor.authorBeura, Samir Kumar
dc.contributor.authorDhapola, Rishika
dc.contributor.authorPanigrahi, Abhishek Ramachandra
dc.contributor.authorYadav, Pooja
dc.contributor.authorReddy, Dibbanti Harikrishna
dc.contributor.authorSingh, Sunil Kumar
dc.date.accessioned2024-01-21T10:55:04Z
dc.date.accessioned2024-08-14T07:44:20Z
dc.date.available2024-01-21T10:55:04Z
dc.date.available2024-08-14T07:44:20Z
dc.date.issued2022-08-01T00:00:00
dc.description.abstractAlzheimer's disease (AD), a progressive neurodegenerative disorder, is considered one of the most common causes of dementia worldwide, accounting for about 80 % of all dementia cases. AD is manifested by the extraneuronal deposition of senile plaques of amyloid beta (A?) and intraneuronal accumulation of neurofibrillary tangles of phosphorylated tau. The impaired proteostasis of these filamentous A? and tau is significantly regulated by reactive oxygen species (ROS). ROS-induced oxidative stress (OS) is the cardinal cause behind neuroinflammation-triggered neurodegeneration during AD. Besides ROS-induced neuro-inflammation, AD is also associated with cerebrovascular dysfunction, where platelet primarily plays a significant role in blood-vessel integrity and tissue repair. Though platelets are the circulatory cell fragments that play predominant roles in thrombosis and hemostasis, their contributions to other physiological functions are also being elucidated. Surprisingly, platelets contribute about 90 % of the circulatory A? and share striking similarities with neurons in several aspects, including different neurotransmitters and their cognate receptors, thus considering platelets as potential peripheral models for AD. Interestingly, platelet structural and functional dysfunctions are evident in AD, where ROS production is associated with platelet hyperactivity. Although activated platelet carries several vital enzymes and immunomodulatory molecules, which can potentially exacerbate OS-mediated neuronal damage, and neurodegeneration, their mechanism of action and mode of progression, are still obscure. Therefore, in this review, we have described the detailed role of OS and platelet in AD, addressing the therapeutic approach and molecular mechanism of platelet-mediated ROS generation as a contributing factor in aggravating the disease. � 2022 Elsevier Inc.en_US
dc.identifier.doi10.1016/j.lfs.2022.120855
dc.identifier.issn243205
dc.identifier.urihttp://10.2.3.109/handle/32116/4329
dc.identifier.urlhttps://linkinghub.elsevier.com/retrieve/pii/S0024320522005550
dc.language.isoen_USen_US
dc.publisherElsevier Inc.en_US
dc.subjectAlzheimer's diseaseen_US
dc.subjectAmyloid betaen_US
dc.subjectBlood plateleten_US
dc.subjectOxidative stressen_US
dc.subjectPhosphorylated tauen_US
dc.subjectReactive oxygen speciesen_US
dc.titleRedefining oxidative stress in Alzheimer's disease: Targeting platelet reactive oxygen species for novel therapeutic optionsen_US
dc.title.journalLife Sciencesen_US
dc.typeReviewen_US
dc.type.accesstypeClosed Accessen_US

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